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ECC > Common intoxications > Flashcards

Common intoxications Flashcards

1
Q

Induction of emesis

A

may remove up to 40-80% of the ingested materia

most effective within 1 hour of ingestion, limited benefit more than 4 hours after ingestion

Requires presence of food in the stomach

CONTRAINDICATED FOR CORROSIVE/CAUSTIC TOXINS AND FOR PETROLEUM DISTILLATES OR IN PATIENTS WITH DEPRESSED MENTAL STATUS OR SEIZURES

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2
Q

Options for inducing emesis

A

Apomorphine (poorly effective in cats)

Xylazine (useful in cats, effective in only 40-75% of cases)

Dexmedetomidine (sedation and resp depression can occur)

Syrup of ipecac and hydrogen peroxide (uncommonly used, irritant effects on gastric mucosa)

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3
Q

Gastric lavage

A

Useful for patients where emesis is ineffective or contraindicated, although requires the patient to be unconscious or anesthetised

CONTRAINDICATED IN FOR CORROSIVE/CAUSTIC TOXINS AND FOR PETROLEUM DISTILLATES and may be ineffective for congealed or “chunky” material.

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4
Q

Potential complications for gastric lavage

A

aspiration, increased transit of the toxin into the small intestine, or potentially electrolyte disturbances or oesophageal trauma.

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5
Q

Activated charcoal administration

A

Acts by adsorption

Most beneficial when given <2h after toxin ingestion, may still be useful up to 24h,

should not be given to patients at risk for aspiration pneumonia or if GI perforation suspected

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6
Q

Cathartics

A

Less commonly used

Enhance elimination of substances - promotes movement through GI tract

Contraindicated if patient is dehydrated or has diarrhoea, ileus, or intestinal obstruction

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7
Q

Types of cathartics

A

Bulk cathartics (metamucil, pumpkin)

Osmotic cathartics (sorbitol)

Lubricant cathartics (mineral oil - reduced efficacy of activated charcoal)

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8
Q

Intralipid infusion

A

treatment of lipophilic toxins

20% fat emulsion for IV infusion

oil in water emulsion, including long-chain and medium chain triglycerides and egg phospholipids

Essentially acts as a “lipid sink” for lipophilic toxins

expected to cause hyperlipidaemia and may cause other adverse effects e.g. pancreatitis and “fat overload syndrome”

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9
Q

Toxin in chocolate

A

Methylxanthines - particularly theobromine and caffeine

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10
Q

Mechanism of chocolate toxicity

A

Inhibit cellular phosphodiesterase
- increase in cyclic AMP
- release of catecholamines

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11
Q

Clinical signs of chocolate toxicity

A

20 mg/kg -> clinical signs,
40-50 mg/kg -> severe signs,
60 mg/kg can cause seizures

CNS/muscle stimulation (hyperactivity, restlessness, incoordination, seizures, tachycardia, and arrhythmias),

diuresis,

vomiting and diarrhoea,

excessive urination,

arrhythmias,

hyperthermia,

incoordination.

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12
Q

Timeframe for chocolate toxicity

A

clinical signs begin within 12h of ingestion and can last up to several days with large ingestions (long half-life)

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13
Q

Treatment of chocloate toxicity

A

Emesis/gastric lavage if recent + activated charcoal (activated charcoal every 3 to 8 hours for up to 72 hours)

Diazepam/phenobarbital may be needed to control seizures and management of arrhythmia may be necessary (lidocaine, propanolol)

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14
Q

Toxin in anticoagulant rodenticides

A

First-generation (e.g., warfarin, pindone),

or

more potent, longer-lasting second-generation (e.g., brodifacoum, bromadiolone, diphacinone, chlorophacinone).

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15
Q

Mechanism in anticoagulant rodenticide toxicity

A

Competitively inhibits vitamin K epoxide reductase which is essential for the formation of coagulation factors II, VII, IX, and X.

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16
Q

Clinical signs in anticoagulant rodenticide toxicity

A

Clinical signs relate to haemorrhage, esp exercise intolerance, lethargy, haemoptysis, intracavitary bleeding.

Mucosal bleeding, petechiation/ecchymosis etc may occur but less common than disorders of primary haemostasis (e.g. immune-mediated thrombocytopaenia)

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17
Q

TImeframe of anticoagulant rodenticide toxicity

A

Whilst absorption is rapid, prolongation of PT/APTT is not observed or measurable for 36-48 hours due to the half-life of factor VII. Clinical signs typically do not develop for 3-5 days.

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18
Q

Treatment of anticoagulant rodenticide toxicity

A

If recent ingestion, reasonable to induce emesis and assess PT/APTT at 36-48h.

If prolonged at that time, vitamin K1 should be administered for 7 (first generation) to 30 (second generation) days and PT/APTT should be reassessed after stopping treatment.

For patients with clinical evidence of haemorrhage, Vit K1 +/- plasma or blood transfusion, and intensive care may be required.

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19
Q

Mechanism of NSAID toxicity

A

Inhibits the activity of cyclooxygenase (COX, mainly COX-1 and -2), reducing conversion of arachidonic acid to prostaglandins, prostacyclins and thromboxane.

COX-1 appears generally has more role in autoregulation/homeostasis whereas COX-2 is more important in the production of inflammatory mediators but COX selectivity is often lost following overdose.

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20
Q

Clinical signs of NSAID toxicity

A

Gastric ulceration (vomiting, haematemesis, melena, abdominal pain) and/or acute kidney injury (PUPD/oliguria/anuria, anorexia, lethargy, and vomiting).

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21
Q

Timeframe of NSAID toxicity

A

Rapidly absorbed but GI signs usually develop within 12 hours, and azotaemia can develop within 24 to 48 hours of ingestion.

22
Q

Treatment of NSAID toxicity

A

Emesis useful if <2h of ingestion.

Activated charcoal + repeated administration useful due to enterohepatic recirculation.

Gastroprotectants (omeprazole or potentially misoprostol) should be prescribed for 7-10 days.

Hospitalisation for IVFT for 48-72 hours is advisable to maintain hydration/perfusion but not prevent kidney injury.

Additional supportive care may be required if renal injury occurs or if significant GI blood loss.

23
Q

Toxin in paracetamol

A

N-acetyl-para-benzoquinoneimine (NAPQI, a toxic metabolite).

NB: CATS MUCH MORE SENSITIVE THAN DOGS due to their low capacity for glucuronidation and sulphation, and their increased susceptibility to erythrocyte oxidative damage.

24
Q

Mechanism of paracetamol toxicity

A

Oxidative damage to erythrocytes leading to Heinz body anaemia.

NAPQI causes the oxidation of ferrous iron (Fe2+) to ferric iron (Fe3+), which converts hemoglobin to methemoglobin and leads to methemoglobinemia.

25
Q

Clinical signs in paracetamol toxicity

A

Cats primarily develop methemoglobinemia, followed by Heinz body anaemia. Methemoglobinemia results in brown or muddy appearing mucous membranes and usually accompanied by tachycardia, hyperpnea, weakness, and lethargy. Facial and paw edema and keratoconjunctivitis sicca also reported.

Dogs tend to more commonly develop liver necrosis, leading to anorexia, lethargy, icterus, GI signs, hepatic encephalopathy etc.

26
Q

Timeframe of paracetamol toxicity

A

Rapidly absorbed. Methemoglobinemia usually develops within a few hours, followed by Heinz body formation. Liver damage usually seen 24–36 hr after ingestion.

27
Q

Treatment of paracetamol toxicity

A

Emesis useful if performed early.

Activated charcoal + repeated administration useful due to enterohepatic recirculation.

Current treatment in dogs and cats is primarily N-acetylcysteine and supportive therapy.

N-acetylcysteine, acts as a glutathione precursor and can therefore reduce the extent of liver injury or methemoglobinemia.

S-adenosylmethionine (SAMe) also useful for cases with hepatic necrosis.

Other treatments are also reported but less commonly used e.g. ascorbic acid, cimetidine, methylene blue.

28
Q

Mechanism of xylitol toxicity

A

Results in an insulin spike -> rapid hypoglycaemia.

In some dogs, this may be followed by acute hepatic necrosis and potentially fulminant liver failure, although the exact mechanism for hepatotoxicity is unknown.

29
Q

Clinical signs of xylitol toxicity

A

dose dependent.

DOGS APPEAR TO BE MUCH MORE SUSCEPTIBLE TO TOXICITY THAN CATS.

Vomiting is a frequent early sign. #

Hypoglycemia (CNS depression, ataxia, recumbency, tremors and seizures)

hepatic necrosis (incr ALT, icterus, V+, lethargy, anorexia, coagulopathy etc)

30
Q

Treatment of xylitol toxicity

A

Emesis can be useful if the patient is euglycaemic but activated charcoal is ineffective.

Aggressive management for hypoglycaemia may be required with IV glucose/dextroxe.

Management of hepatic necrosis/failure centres on supportive care and use of anti-oxidants (e.g. SAMe).

31
Q

Mechanism of ethylene glycol toxicity

A

Metabolised to several toxic metabolites including glycoaldehyde, glycolic acid, and oxalic acid -> calcium oxalate crystalluria -> AKI.

32
Q

Clinical signs and timeframe of ethylene glycol toxicity

A

30 minutes to 12 hours: Ataxia, hypersalivating, vomiting (Looks similar to alcohol poisoning).

12-24 hours: Clinical signs seems to be improving but severe renal injury is occurring. Signs of dehydration, tachycardia, and tachypnoea may occur.

12-24 hours (cats) or 36-72 hours (dogs): Severe AKI occurs with anorexia, depression, uraemia, vomiting etc +/- oliguria/anuria.

33
Q

Treatment of ethylene glycol poisoning

A

An ethylene glycol test is available but is only accurate within approximately the first 24 hours after ingestion prior to metabolism.

Antidote therapy: Fomepizole or ethanol can be given within 8-12 hours of exposure in dogs and within 3 hours in cats. Fomepizole is preferred but difficult to obtain. Ethanol (e.g. vodka or grain alcohol) is administered IV

Treatment of AKI involved intensive IV fluid therapy, urine output monitoring and supportive care; however, once azotaemia has already developed, the prognosis is generally poor to grave.

34
Q

Mechanism of propylene glycol toxicity

A

Metabolised to both D- and L-lactic acid, potentially leading to metabolic acidosis.

35
Q

Clinical signs of propylene glycol toxicity

A

Relatively rare; however, >5g/kg daily can lead to hemolytic anemia, reticulocytosis, and hyperbilirubinemia in dogs.

Cats seem to be more sensitive may develop dose-related increases in Heinz bodies at lower doses

Clinical signs may include CNS depression/ataxia and tachypnoea due to metabolic acidosis, haematological changes, PUPD, cardiovascular collapse, and, in cats, muscle twitching or hypotension.

36
Q

Timeframe of propylene glycol toxicity

A

clinical signs develop following chronic exposure over weeks/months.

37
Q

Treatment for propylene glycol toxicity

A

Generally supportive (IVFT, haematological monitoring, blood transfusion if indicated).

38
Q

Toxin in marijuana toxicity

A

tetrahydrocannabinol (THC) plus other cannabinoids

39
Q

Mechanism of marijuana toxicity

A

THC is highly lipophilic and distributes to brain and other fatty tissues following absorption.

Binds to cannabinoid receptors mainly in CNS but also in other tissues e.g. lungs, liver and kidneys.

NB: substantial first-pass effect following ingestion. Generally has a wide margin of safety so death is uncommon.

40
Q

Clinical signs of mariujana toxicity

A

CNS depression/ disorientation/ behavioural changes,
ataxia,
“glassy eyes”,
mydriasis,
recumbency,
hypothermia,
bradycardia,
urinary incontinence.

In cats,
“fly biting” behaviours are relatively common.
Vomiting,
diarrhoea
seizures

41
Q

Timeframe for marijuana toxicity

A

Clinical signs can occur within 6-12 minutes after inhaling smoke and 30-60 minutes after ingestion.

42
Q

Treatment for marijuana toxicity

A

Supportive care (e.g. monitoring of temperature, pulse and respiration rates, IVFT) until resolution of clinical signs.

Emesis can be useful if ingestion has occurred recently (<30 mins) and CNS depression is not present.

Activated charcoal + repeated administration is useful due to enterohepatic recirculation.

43
Q

Toxin in lillies (cats)

A

Unknown

44
Q

Mechanism in lilly toxicity (cats)

A

Associated with development of acute kidney injury (AKI) in CATS.

45
Q

Clinical signs of lily toxicity in cats

A

Hypersalivation and vomiting is common within minutes to hours following ingestion.

The vomiting often resolves/subsides within a few hours of ingestion but AKI develops within 12-72 hours.

Oliguric to anuric renal failure may develop, normally accompanied by vomiting, depression, anorexia, dehydration, and/or hypothermia.

Approximately 1/3 of cats may also develop ataxia, depression, tremors, seizures, head pressing, and other neurological signs.

45
Q

Timeframe of lily toxicity (cats)

A

Hypersalivation and vomiting typically occurs rapidly (within minutes-hours) with AKI occurring between 12h-72h following ingestion.

46
Q

Treatment of lily toxicity in cats

A

Emesis useful if ingestion is recent and no contraindications are present.

Activated charcoal is also useful to reduce toxin absorption.

Treatment is otherwise supportive (IVFT, close monitoring of urine output/electrolytes, antiemetic therapy etc.)

Prognosis is related to rapidity of diagnosis and treatment.

Treatment delays of >18 hours usually are associated with development of severe renal failure and death.

47
Q

Toxin in raisin and grape toxicity in dogs

A

The causative toxin is unknown and the exact amount of ingested fruits necessary to cause damage seems to be variable.

48
Q

Mechanism of raisin and grape toxicity in dogs

A

Associated with development of acute kidney injury (AKI) in DOGS

49
Q

Clinical signs and timeframe of raisin and grape toxicity in dogs

A

Vomiting, diarrhoea, inappetence may occur within 6-12 hours of ingestion with AKI developing within 24-72 hours.

Marked CNS signs may occur shortly following ingestion but are not associated with the severity of azotaemia and usually regress over days to weeks.

50
Q

Treatment of raisin and grape toxicity in dogs

A

Emesis if recent ingestion and activated charcoal.

Treatment for AKI is supportive and prognosis poor if patients are anuric/oliguric.

In asymptomatic patients with a history of raisin/grape ingestion, urea and creatinine concentrations should be assessed daily for at least three days for evidence of AKI.

ECC (8 decks)

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